Hypertension is a major public health concern. An estimated 30-40% of the adult population in the developed world suffers from this condition. Diagnosis and treatment of hypertension remain suboptimal. Despite the availability of numerous safe and effective pharmacological therapies, the percentage of patients achieving adequate blood-pressure control to guide-line target values remains low. Much failure of the pharmacological strategy to attain adequate blood-pressure control is attributed to both physician inertia and patient non-compliance and non-adherence to a lifelong pharmacological therapy. Thus, the development of new approaches for the management of hypertension is a priority. These considerations are especially relevant to patients with so-called resistant hypertension (i.e., those unable to achieve target blood-pressure values despite multiple drug therapies at the highest tolerated dose). Such patients are at high risk of major cardiovascular events.
Renal sympathetic efferent and afferent nerves, which lie within and immediately adjacent to the wall of the renal artery, are crucial for initiation and maintenance of systemic hypertension. Indeed, sympathetic nerve modulation as a therapeutic strategy in hypertension had been considered in the past. Surgical methods for thoracic, abdominal, or pelvic sympathetic denervation had been successful in lowering blood pressure in patients with so-called malignant hypertension. However, these methods were associated with high perioperative morbidity and mortality and long-term complications, including bowel, bladder, and erectile dysfunction, in addition to severe postural hypotension. Renal denervation is the application of a chemical agent, or a surgical procedure, or the application of energy to partially or completely damage renal nerves to partially or completely block renal sympathetic nerve activity. Renal denervation reduces or completely blocks renal sympathetic nerve activity, increases renal blood flow, decreases renal plasma norepinephrine content, and reduces the release of renin into the systemic circulation.
The objective of renal denervation is to neutralize the effect of excess renal sympathetic nerve activity which is involved in both arterial hypertension and heart failure. Device-based renal denervation is known in the art. For example, U.S. Patent Application Publication 2011/0118726 titled “Assembly of Staggered Ablation Elements,” the contents of which are hereby incorporated by reference herein, describes a catheter based renal denervation device featuring a catheter with an expandable structure connected to the distal end of the catheter. Once the device is located at the desired position within a renal artery or vein, ablation elements connected to the expandable structure can be energized to ablate the desired renal nerves or to otherwise block nerve activity.
Current devices for renal denervation utilize metallic electrodes to apply a radiofrequency (“RF”) electrical field to resistively heat the adjacent arterial endothelium. Subsequent heat transfer across the arterial wall, from endothelium to adventitia, results in denervation of the renal nerve. Procedural damage to the renal artery endothelium during a renal denervation process can be undesirable since the subsequent healing response may result in stenosis. Direct exposure of the endothelium to the RF electric field may also result in irreversible electroporation and surface electrolysis. This is because RF fields can have concentrated effects at the tissue surface which are more concentrated than heat transfer to the tissue surface.
Additionally, partial contact of the electrode may expose the circulating blood flow to the concentrated resistive heating zone resulting in coagulation, charring of the electrode surface, and increasing the potential for thrombus formation.
Thus, further improvement of devices and methods for renal denervation would be desirable.